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DEVELOPMENT OF SEROTONERGIC AND ADRENERGIC RECEPTORS IN THE RAT SPINAL CORD: EFFECTS OF NEONATAL CHEMICAL LESIONS AND HYPERTHYROIDISM
Citation:
Lau, C., A. Pylypiw, AND L. Ross. DEVELOPMENT OF SEROTONERGIC AND ADRENERGIC RECEPTORS IN THE RAT SPINAL CORD: EFFECTS OF NEONATAL CHEMICAL LESIONS AND HYPERTHYROIDISM. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-85/085 (NTIS PB85239408), 1985.
Description:
The ontogeny of serotonergic receptors and alpha- and beta-adrenergic receptors in thoracolumbar spinal cord of rats given neurotoxins which destroy serotonergic (5,7-dihydroxytryptamine (5,7-DHT) or noradrenergic (6-hydroxydopamine (6-OHDA)) nerve terminals was examined. Intracisternal administration of 5,7-DHT or 6-OHDA at 1 and 6 days of age prevented, respectively, the development of 5-HT and CA levels in the spinal cord. Rats lesioned with 5,7-DHT displayed a marked elevation of 5-HT receptors with a binding of 50% greater than controls at 1 week and a continuing increase to twice normal by 4 weeks. A similar pattern of up-regulation was also detected with the alpha-adrenergic receptor, as rats lesioned with 6-OHDA exhibited persistent increases in receptor concentration. However, in these same animals ontogeny of the beta-adrenergic receptor in the spinal cord remained virtually unaffected by the chemical lesion. Neonatal treatment of triiodothyronine on the other hand was capable of evoking persistent increases in beta-adrenergic receptor binding.